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Topic: IgE (Read 4611 times)

I recently took a blood test antibody assesment and it revealed that my IgE level is freakishly high.I have a hyperactive immune system, as I'm sure most of us do. However, my IgG food allergy results concluded that I only have minor allergies (to most foods though).

Does anybody have any advice on how one can lower their IgE levels by use of natural means?

DHEA - this hormone is available as an OTC dietary supplement in the USA.┬ If you Google for DHEA and inflammation or anti-inflammatory there's quite a few interesting articles.┬ Women, in particular, should only take very small amounts unless under medical supervision.

http://www.lef.org/protocols/metabolic_health/dhea_replacement_01.htmDHEA: Fighting Inflammation Inflammation is an insidious condition, and we are learning more every year about its association with a host of diseases. Inflammation is caused by internal chemicals called inflammatory cytokines that are released as part of the immune system response. These chemicals, including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin 1(beta) [IL-1(β)] and/or leukotriene, are present in greater concentrations as we age. Reducing the concentration of inflammatory cytokines to reduce the risk of serious disease is one goal of nutrient and hormone therapy.

Dehydroepiandrosterone (DHEA) and its sulfate derivatives are known to affect host immune function; however if such hormones influence the development of atopic dermatitis has not yet been clarified. In this study, we examined the effects of DHEA on the allergic process using NC/Nga mouse, a model animal of human atopic dermatitis. The administration of DHEA profoundly suppressed the spontaneous elevation of both serum IgE and interleukin-6 levels in NC/Nga mice during the observation period. These results indicate that DHEA promotes a shift in Thl/Th2 balance toward Th1-dominant immunity, and thus may be one of the effective alternatives in treating atopic dermatitis.

Department of Dermatology, Tohoku University, School of Medicine, Sendai, Japan.

Previous studies in mice have shown that dehydroepiandrosterone (DHEA) increases the production of Th1-associated lymphokines, and of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma), by lymphocytes. However, there are no reports concerning the effect of DHEA on the production of Th2-associated lymphokines, IL-4 and IL-5, by lymphocytes in humans. We examined serum DHEA levels in patients with atopic dermatitis (AD), which is thought to be associated with a higher activity of Th2 cells than of Th1 cells. We also studied the effects of DHEA on the production of IL-4 and IL-5 by human lymphocytes. Serum DHEA concentrations in 47 adult male patients with AD aged 19-30 years were significantly lower than those of 53 age-matched healthy male controls. Preincubation of peripheral blood mononuclear cells (PBMCs) with DHEA reduced the IL-4 production by concanavalin A-stimulated PBMCs. Their IL-5 production also showed a tendency to decrease. These results suggest that DHEA may be one of the regulators of IgE synthesis and eosinophil proliferation in patients with AD and it may act by controlling IL-4, IL-5 and IL-2 production by lymphocytes.

High oral doses of vitamin C have been used safely for decades. If the amount you are using causes diarrhea, the dosage needs to be reduced. However, in some conditions, in order for vitamin C to be effective it has to be used in doses that come very close to causing diarrhea. Unless this "bowel tolerance" dose is found and maintained, the condition for which the vitamin C was recommended may not resolve. If you are consuming doses of vitamin C greater than perhaps 500mg per day, do not stop its use abruptly. It is best to taper your dose down over several days. A sudden reduction may result in a temporary deficit ("rebound scurvy") and a negative influence on your resistance to infection.

Omega 3 essential fatty acids in the form of fish oil or flaxseed oil are anti-inflammatory

Hydrogenated oils and trans-fats are inflammatory and need to be eliminated from the diet and the Omega 3 essential fatty acids should be increased. Omega-3s are found in fish oil and flax seed oil, though most people are inefficient converters of the ALA in flax to the essential EPA and DHA, so it's usually better to take fish oil. (Or eat lots of cold water fish, but watch out for the mercury levels)

BACKGROUND: Atopic dermatitis is a common chronic skin disorder characterized by inflammation and itching. It is frequently seen in people with a personal or family history of asthma and allergic rhinitis. Some research has shown that vitamin E can lower blood levels of IgE (immunoglobulin E), a key immune factor involved in allergic reactions, suggesting that the vitamin may have a potential role in reducing allergic symptoms.

RESEARCH: Researchers asked 96 patients with atopic dermatitis to take either 400 IU of natural-source vitamin E or placebos daily for eight months. Among the initial symptoms were facial redness, thickening of the skin, eczema, and itching.

RESULTS: Patients taking vitamin E supplements had significant improvements compared with those taking placebos. Seven of the patients taking vitamin E had nearly complete remissions of atopic dermatitis compared with none in the placebo group. Overall, 23 people taking vitamin E experienced "great improvement" and 10 had slight improvement. In contrast, only one patient taking placebos had a great improvement and four had slight improvements. Only four patients taking vitamin E actually worsened during the study, compared with 36 in the placebo group. IgE levels decreased by 62 percent in the vitamin E group who experienced great improvement or remission, but only 34.4 percent in the placebo group.

IMPLICATIONS: This study showed a strong trend toward improvement from vitamin E supplements, although not every patient benefited. The researchers concluded, "Our findings suggest that vitamin E may play an important role in IgE-mediated atopic responses in humans by significantly decreasing the serum IgE levels. This leads to an improvement in clinical symptoms, offering patients a better quality of life and dermatologists a safe tool for the treatment of atopic dermatitis."

Tsoureli-Nikita E, Hercogova J, Lotti T, et al, ┼ôEvaluation of dietary intake of vitamin E in the treatment of atopic dermatitis: a study of the clinical course and evaluation of the immunoglobulin E serum levels,┬Ł International Journal of Dermatology, 2002;41:146-150.

A deficiency of D is associated with auto-immune diseases. Since Vitamin D is produced in the skin on exposure to UVB sunlight, many of us who live away from the equator become Vitamin D deficient during the winter or if we habitually avoid sun exposure. Cod Liver oil is a good source of D ( in capsules for those of us who can't stand the taste) in the winter.

For those who do not fear the sun, judiciously expose as much skin as possible to direct midday sunlight for 1/4 the time it takes for their skin to turn red, during those months when the proper ultraviolet light occurs at their latitude (usually late spring, summer and early fall). Do not get sunburned. Vitamin D production is already maximized before your skin turns pink and further exposure does not increase levels of vitamin D but may increase your risk of skin cancer. Black patients may need five to ten times longer in the sun than white patients, depending on skin type. http://www.vitamindcouncil.com/treatment.shtml

http://www.vitamindcouncil.com/vdds.shtmlVitamin D Deficiency SyndromeJohn Jacob Cannell, MD27 December 2003AbstractWe propose Vitamin D Deficiency Syndrome, or VDDS, exists when 25(OH)D levels of less than 25 ng/ml are found in patients with two or more of the following conditions: osteoporosis, heart disease, hypertension, autoimmune diseases, certain cancers, depression, chronic fatigue or chronic pain. VDDS is more common among dark skinned races, the aged and those who avoid the sun.

Serum 25(OH)D levels are obtained when the disorder is suspected. Serum 1,25 (OH)D levels have no place in diagnosing the syndrome and will mislead the physician. Sunlight, artificial light, oral or parental vitamin D, or a combination, aimed at restoring circulating levels of 25(OH)D between 35 and 55 ng/ml is the treatment of choice. Controlled sunlight is the safest form of vitamin D repletion. Cholecalciferol is the preferred form of oral vitamin D.

Vitamin D is safe when used in physiological doses (those used by Nature). Physiological doses are 3,000-5,000 IU/day, from all sources (sun, diet and supplements). Should hypercalcemia occur with such doses, it is due to vitamin D hypersensitivity syndrome, not vitamin D toxicity. Vitamin D hypersensitivity syndromes include conditions such as primary hyperparathyroidism, occult cancers (especially lymphoma) or granulomatous disease (especially sarcoidosis). In such cases, treatment of vitamin D deficiency should be done under the care of a knowledgeable physician. A serum 25(OH)D, serum 1,25(OH)D, PTH and SMA will lead the clinician in the right direction.